Residency · Residency · Cardiothoracic Surgery

Pericardial Disease: Pericardiectomy and Management

Introduction

The pericardium serves as a protective sac surrounding the heart, composed of an outer fibrous layer and an inner serous layer. Pericardial diseases encompass a spectrum of conditions including acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis. While many pericardial conditions are managed medically, pericardiectomy remains the definitive treatment for constrictive pericarditis and recurrent symptomatic effusions refractory to less invasive approaches.

Anatomy and Physiology of the Pericardium

The normal pericardial sac contains 15-50 mL of serous fluid serving as lubrication. The pericardium limits acute cardiac dilation, maintains ventricular coupling, and reduces friction. The pericardial compliance curve is steep: once the reserve volume is exceeded, small additional fluid volumes cause rapid pressure increases. Chronic effusions allow gradual pericardial stretching, tolerating volumes of 1-2 liters before hemodynamic compromise. The pericardium is not essential for life, and congenital absence and surgical removal are well-tolerated.

Acute Pericarditis

Etiology

Idiopathic and viral causes account for 80-90% of cases in developed countries, with common viral pathogens including Coxsackievirus, echovirus, adenovirus, CMV, and HIV. Post-cardiac injury syndromes include postpericardiotomy syndrome after cardiac surgery and Dressler syndrome following myocardial infarction. Autoimmune causes include SLE, rheumatoid arthritis, scleroderma, and sarcoidosis. Tuberculous pericarditis is the leading cause in endemic regions, and bacterial (purulent) and fungal infections also occur. Other etiologies include uremic, neoplastic (lung, breast, lymphoma, melanoma), radiation-induced, and drug-induced pericarditis.

Diagnosis and Management

The classic presentation includes sharp pleuritic chest pain relieved by sitting forward, a pericardial friction rub, and diffuse ST elevation with PR depression on ECG. Elevated inflammatory markers (CRP, ESR) support the diagnosis. Echocardiography assesses for effusion and tamponade physiology. First-line treatment consists of NSAIDs (ibuprofen 600 mg three times daily) plus colchicine (0.5 mg twice daily) for 3 months. Colchicine reduces recurrence by 50% as demonstrated by the COPE and CORP trials. Corticosteroids are reserved for refractory cases, autoimmune etiologies, or contraindications to NSAIDs and colchicine, and are associated with higher recurrence when used first-line.

Pericardial Effusion and Cardiac Tamponade

Pathophysiology of Tamponade

Cardiac tamponade occurs when intrapericardial pressure exceeds intracardiac diastolic pressures, impairing ventricular filling. The rate of fluid accumulation matters more than the volume: rapid accumulation of 150-200 mL can cause tamponade, while chronic effusions may tolerate over 1 liter. Beck's triad (hypotension, muffled heart sounds, JVD) is classic but often incomplete. Pulsus paradoxus, defined as a drop in systolic BP exceeding 10 mmHg with inspiration, is the most sensitive clinical sign. Echocardiographic findings include right atrial systolic collapse, right ventricular diastolic collapse, respiratory variation in mitral and tricuspid inflow velocities, and IVC plethora.

Pericardiocentesis

Emergency pericardiocentesis is life-saving for hemodynamically significant tamponade. It is performed under echocardiographic or fluoroscopic guidance via the subxiphoid approach. Drainage of as little as 50 mL can produce dramatic hemodynamic improvement. A catheter is left in place for continued drainage until output falls below 25-50 mL per day. Fluid is sent for cell count, cytology, culture, protein, glucose, LDH, and adenosine deaminase if tuberculosis is suspected.

Surgical Drainage Options

The subxiphoid pericardial window is performed under local or general anesthesia and allows both biopsy and drainage. VATS pericardial window provides excellent visualization and tissue sampling through a thoracoscopic approach. Balloon pericardiotomy is a percutaneous method for creating a pleuropericardial communication, used primarily for malignant effusions. Indications for surgical drainage include loculated effusions, need for tissue biopsy, recurrent effusions after pericardiocentesis, and purulent pericarditis.

Constrictive Pericarditis

Pathophysiology

Chronic inflammation leads to pericardial thickening, fibrosis, and often calcification. The rigid pericardium restricts diastolic filling, causing ventricular interdependence and equalization of diastolic pressures across all chambers. Dissociation of intrathoracic and intracardiac pressures is the hallmark hemodynamic finding. Constrictive pericarditis must be distinguished from restrictive cardiomyopathy, which has a similar clinical presentation but fundamentally different treatment.

Etiology

Post-cardiac surgery is the most common cause in developed countries, accounting for 30-40% of cases. Idiopathic and viral causes account for another 30-40%. Post-radiation therapy, especially mediastinal radiation for Hodgkin lymphoma, is an important etiology. Tuberculous pericarditis is the leading cause worldwide. Connective tissue disease, uremia, trauma, and neoplastic involvement are less common causes.

Diagnosis

Clinical features include progressive dyspnea, peripheral edema, ascites out of proportion to peripheral edema, and hepatomegaly. Kussmaul sign is a paradoxical rise in JVP with inspiration. A pericardial knock is an early diastolic sound characteristic of constriction. Echocardiography demonstrates septal bounce, respiratory variation in mitral inflow exceeding 25%, and annulus reversus (medial e' greater than lateral e'). Cardiac MRI reveals pericardial thickening exceeding 4 mm, and late gadolinium enhancement of the pericardium indicates active inflammation. Cardiac catheterization shows equalization of diastolic pressures, a square root sign, and discordance of RV and LV pressures with respiration. CT chest may demonstrate pericardial calcification, which is pathognomonic but present in only 25-30% of cases.

Pericardiectomy

Indications

The definitive indication for pericardiectomy is constrictive pericarditis with symptomatic heart failure refractory to medical therapy. Other indications include recurrent pericardial effusions despite medical therapy and repeated drainage, purulent pericarditis with loculation not amenable to catheter drainage, and effusive-constrictive pericarditis with persistent constriction after drainage.

Surgical Technique

Median sternotomy is the preferred approach, providing access to both ventricles and the great vessels. Cardiopulmonary bypass should be on standby and is used in 10-20% of cases for hemodynamic instability or ventricular injury. Radical pericardiectomy involves resection of the pericardium from phrenic nerve to phrenic nerve, including the diaphragmatic pericardium. Dissection begins over the least adherent area, usually the LV free wall, and extends to the right. Sharp dissection is preferred to minimize myocardial injury, and the epicardial plane must be identified carefully. Calcified pericardium adherent to the epicardium may require leaving islands of calcium to avoid ventricular perforation.

Outcomes

Operative mortality is 5-10% overall, higher in radiation-induced constriction at 15-20% and in patients with advanced NYHA class. Symptomatic improvement occurs in 70-80% of patients. Radiation-induced constrictive pericarditis has the worst outcomes due to concurrent myocardial fibrosis and valvular disease. Low cardiac output syndrome may occur postoperatively as the chronically underfilled ventricle suddenly dilates. Long-term survival is excellent when underlying myocardial function is preserved, with 5-year survival of approximately 70-80%.

Constrictive vs. Restrictive: Distinguishing Features

Key Clinical Pearls

Colchicine should be part of first-line therapy for acute pericarditis, as it halves the recurrence rate and is supported by robust trial data. The rate of pericardial fluid accumulation, not the volume, determines hemodynamic significance, and even small acute effusions can cause tamponade. Constrictive pericarditis is curable with pericardiectomy, but radiation-induced constriction carries significantly worse surgical outcomes due to concurrent myocardial and valvular disease. The distinction between constrictive pericarditis and restrictive cardiomyopathy is critical because their treatments are diametrically opposed: surgery for constriction versus medical therapy or transplant for restriction. Transient constrictive pericarditis with active pericardial inflammation demonstrated by MRI enhancement may resolve with anti-inflammatory therapy, avoiding surgery.

References

1. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the Diagnosis and Management of Pericardial Diseases. Eur Heart J. 2015;36(42):2921-2964.
2. Imazio M, Brucato A, Cemin R, et al. A Randomized Trial of Colchicine for Acute Pericarditis. N Engl J Med. 2013;369(16):1522-1528.
3. Depboylu BC, Mootoosamy P, Vistarini N, et al. Surgical Treatment of Constrictive Pericarditis. Tex Heart Inst J. 2017;44(2):101-106.
4. Welch TD, Oh JK. Constrictive Pericarditis: Old Disease, New Approaches. Curr Cardiol Rep. 2015;17(4):20.

Read this lecture as Markdown